We report a 55-year-old man who experienced proximal muscle weakness accompanied by the atrial flutter (AFL) with 1:1 conduction. Detailed examination revealed elevated antimitochondrial antibodies (AMA) and creatine kinase (CK). AFL was converted to sinus rhythm by cardioversion. He was diagnosed as AMA-positive myositis-associated AFL and was treated by prednisolone. Although his muscle weakness and CK level improved, AFL with 1:1 conduction reappeared. Therefore, radiofrequency catheter ablation (RFCA) was needed to treat the AFL, resulting in maintenance of sinus rhythm. This case report describes cardiac involvement in a patient with AMA-positive myositis.
We herein report an adult case of unicommissural unicuspid aortic valve (UAV). A 59-year-old man, who was noted to have a cardiac murmur at 31 years of age, was admitted to our hospital due to acute heart failure. Severe calcification in the aortic valve with severe low-flow/low-gradient aortic stenosis and moderate aortic regurgitation was observed and thought to be the cause of heart failure, however, the etiology of aortic valve dysfunction was not clear. Aortic valve replacement was subsequently performed, and unicommissural UAV was diagnosed according to the intraoperative findings. UAV is very rare congenital aortic valve disease which is rarely diagnosed preoperatively.
We herein report the case of a 55 year-old male who underwent pulmonary vein isolation (PVI) for paroxysmal atrial fibrillation. From 8 months after PVI, exertional dyspnea rapidly appeared. When he was referred to our hospital, massive pericardial effusion was observed by transthoracic echography. The pericardiocentesis revealed bloody pericardial effusion, and improved symptoms. Although aortic dissection, autoimmune disease, infection, metastatic pericardial tumor, primary pericardial tumor, and malignant neoplasm were considered as differential diagnosis, the cause of pericardial effusion failed to be found. From these findings, the cause of hemorrhagic pericardial effusion was considered delayed cardiac tamponade induced by PVI performed 8 months earlier.
Infection with the varicella zoster virus (VZV) causes two distinct clinical syndromes, varicella and herpes zoster. Primary infection with VZV results in varicella, characterized by viremia with a diffuse rash and seeding of multiple sensory ganglia, where the virus establishes lifelong latency. Endogenous reactivation of latent VZV typically results in a localized skin infection known as herpes zoster. VZV may cause various complications such as secondary bacterial infection, pneumonia, acute cerebellar ataxia, meningitis, encephalitis, and Reye syndrome [1,2]. In contrast, the occurrence of myopericarditis is extremely rare [2]. The occurrence of concurrent myopericarditis with herpes zoster, as in the present case, is extremely rare [3-5]. This article describes a case of pericarditis caused by herpes zoster. Case report We report the case of a 53-year-old immunocompetent male who developed pericarditis caused by herpes zoster. The patient had no particular past history except for varicella in his childhood. Six hours prior to consultation, the patient suddenly noticed chest pain at rest without physical disorders before chest pain developed. At the time of consultation, the patient had a blood pressure of 134/92 mmHg, heart rate of 110 beats per minute, and body temperature of 37.6 C. There was no paradoxical pulse observed. Heart sounds were slightly distant and muffled with no sound of pericardial friction. The jugular venous distension was not observed, and there was no edema of the legs. No rash was observed on the body surface. However, the chest pain persisted. The 12-lead electrocardiography (ECG) revealed concave upward ST segment elevation in the leads of I, II, aVL, aVF, and V1-6 without mirror-image changes and PR segment depression (Fig. 1A). Blood tests revealed a white blood cell count of 11.5 Â 10 3 /mL [normal range (NR), 3.6-8.7 Â 103/mL] and C-reactive protein (CRP) of 1.27 mg/dL (NR, 0.00-0.17 mg/dL) both of which were slightly elevated. Myocardial enzyme was normal with the creatine kinase/ creatine kinase-myocardial band level of 158/80 IU/L (NR, 110-318/ 0-12 IU/L) and troponin I level of 0.02 ng/mL (NR, 0.00-0.04 ng/ mL). Renal function was normal with a creatinine level of 0.78 mg/ dL (NR, 0.65-1.07 mg/dL). The human immunodeficiency virus antibody (types 1, 2) and antigen (type p24) evaluated by chemiluminescent enzyme immunoassay test were negative (NR, negative). Transthoracic echocardiography (TTE) revealed left ventricular ejection fraction of 67%, indicating normal left
We report on an 84-year-old woman with anteroseptal acute myocardial infarction. Emergency coronary angiography revealed the occlusion of proximal left anterior descending artery without collateral circulation, and percutaneous coronary intervention was performed. Two drug eluting stents were implanted, and the procedure was concluded with thrombolysis in myocardial infarction grade 3 without complications. Postoperatively, no murmur was audible on auscultation and no shunt flow was observed on transthoracic echocardiography (TTE), and normal blood pressure was maintained. On day 2, however, the patient's vital signs deteriorated to a state of shock and systolic murmur appeared at the apical region. TTE showed a left-to-right shunt in the apical septal region, and ventricular septal perforation was diagnosed. Although emergency surgery was considered, the patient's vital signs improved the following day. The disappearance of the cardiac murmur and the shunt was confirmed. The clinical course was uneventful thereafter, and the patient was discharged.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.